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Data of gene expressions induced by the interaction between Kupffer cells and cancer cells dependently on Dectin-2

ABSTRACT: Metastasis to distal organ is a fatal cause of cancer death and liver is one of the most common site of metastasis leading to bad prognosis. Although it has been known that innate immune cells play critical roles in the regulation of liver metastasis, how they control the tumor development is still largely unclear. We found that Dectin-2 (Clec4n), a C-type lectin receptor (CLR), suppresses liver metastasis and such Dectin-2-mediated anti-tumor rejection requires Kupffer cells, liver-residing macrophages, which express Dectin-2 dominantly in liver. We used microarray to examine comprehensive gene expressions induced by Dectin-2 when anti-tumoral Kupffer cells interact with cancer cells

ORGANISM(S): Mus musculus

PROVIDER: GSE88809 | GEO | 2016/10/18

SECONDARY ACCESSION(S): PRJNA348714

REPOSITORIES: GEO

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Project description:Kupffer cells have been implicated in the pathogenesis of various liver diseases. However, their involvement in metabolic disorders of the liver, including fatty liver disease, remains unclear. The present study sought to determine the impact of Kupffer cells on hepatic triglyceride storage and to explore the possible mechanisms involved. To that end, C57Bl/6 mice rendered obese and steatotic by chronic high-fat feeding were treated for 1 week with clodronate liposomes, which cause depletion of Kupffer cells. Loss of expression of marker genes Cd68, F4/80, and Clec4f, and loss of Cd68 immunostaining verified almost complete removal of Kupffer cells from the liver. Also, expression of complement components C1, the chemokine (C-C motif) ligand 6 (Ccl6), and cytokines interleukin-15 (IL-15) and IL-1beta were markedly reduced. Importantly, Kupffer cell depletion significantly decreased liver triglyceride and glucosylceramide levels concurrent with increased expression of genes involved in fatty acid oxidation including peroxisome proliferator-activated receptor alpha (PPARalpha), carnitine palmitoyltransferase 1A (Cpt1alpha), and fatty acid transport protein 2 (Fatp2). Treatment of mice with IL-1beta decreased expression of PPARalpha and its target genes, which was confirmed in primary hepatocytes. Consistent with these data, IL-1beta suppressed human and mouse PPARalpha promoter activity. Suppression of PPARalpha promoter activity was recapitulated by overexpression of nuclear factor kappaB (NF-kappaB) subunit p50 and p65, and was abolished upon deletion of putative NF-kappaB binding sites. Finally, IL-1beta and NF-kappaB interfered with the ability of PPARalpha to activate gene transcription. CONCLUSION: Our data point toward important cross-talk between Kupffer cells and hepatocytes in the regulation of hepatic triglyceride storage. The effect of Kupffer cells on liver triglycerides are at least partially mediated by IL-1beta, which suppresses PPARalpha expression and activity. Expression profiling of livers from mice fed control, low-fat diet diet or high-fat diet for 20weeks with or without knockdown of Kupffer cells.

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Data of gene expressions induced by the interaction between Kupffer cells and cancer cells dependently on Dectin-2

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